Figure 6. Inhibition of the AMPK pathway abolishes the protective effect of CTRP9 against VSMC-derived foam cell death. Human aortic smooth muscle cells (HASMCs) were treated for 72 h with 5 µg/mL cyclodextrin-cholesterol complex to establish VSMC-derived foam cells, which were then treated with CTRP9 (10 μg/mL) and ox-LDL (10 μg/mL) in the presence of Compound C or DMSO for 24 h. (a) Western blotting was performed to examine the protein levels of GCLC, Foxo3, GCLM, HO1, SOD2, and NQO1. (b) Quantitative analysis of the oxidant-related protein expression. (c) Mitochondrial ROS levels were detected using a MitoSOX™ Red mitochondrial superoxide indicator. (d) A JC-1 staining kit was used to detect mitochondrial membrane potential. (e) Western blotting was performed to examine the protein levels of MLKL, p-MLKL, RIP3, RIP1, and p-RIP1. (f) Quantitative analysis of necroptosis-associated protein expression. Data are presented as mean ± SD of three independent experiments. ##p < 0.01 vs. the ox-LDL + 10 μg/mL CTRP9 group.